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Sr Director: La enfermedad cardiovascular es la causa más frecuente de muerte en enfermos trasplantados a largo plazo, por lo que es importante incidir en factores de riesgo como la hiperlipemia. En la etiología de la hipertrigliceridemia influyen la obesidad, diabetes mellitus, medicamentos (tacrolimus, β-bloqueantes, corticoesteroides,...), consumo de alcohol, hipotiroidismo, insuficiencia renal, síndrome nefrótico e infección por VIH1. Hipertrigliceridemias entorno a 2000 mg/dL casi siempre son secundarias o de origen familiar.
To the editor: Cardiovascular disease is the most common cause of mortality in long-term transplant recipients; it is therefore important to address associated risk factors such as hyperlipidemia. The etiology of hypertriglyceridemia is influenced by obesity, diabetes mellitus, drugs (tacrolimus, β-blockers, corticosteroids, etc., alcohol consumption, hypothyroidism, renal failure, nephrotic syndrome and HIV infection.1 Hypertriglyceridemia in the order of 2000 mg/dl is almost always of a secondary or familial origin.
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To the editor: Cardiovascular disease is the most common cause of mortality in long-term transplant recipients; it is
therefore important to address associated risk factors such as hyperlipidemia. The etiology of hypertriglyceridemia is influenced by obesity, diabetes mellitus, drugs (tacrolimus, β-blockers, corticosteroids, etc., alcohol consumption,
hypothyroidism, renal failure, nephrotic syndrome and HIV infection.1 Hypertriglyceridemia in the order of 2000
mg/dl is almost always of a secondary or familial origin.
Heparin is widely used as effective prophylaxis and treatment in patients with thrombosis. Independently of its
anticoagulant action, the administration of heparin gives rise to two opposite phenomena regarding the effect of the
drug on the patient lipid profile, derived from its action upon lipoprotein lipase: in the first hour, heparin stimulates the enzyme2 and reduces the triglyceride levels, while posteriorly the enzyme is inhibited and the triglyceride levels consequently increase.3 Although controversial, a number of studies have reported the favorable effects of low molecular weight heparins (LMWHs) upon lipid profile.4,5
We report the case of a 37-year-old male with a history of arterial hypertension, hypercholesterolemia, terminal
chronic renal failure secondary to reflow nephropathy and a first kidney transplant in 1984, with a return to hemodialysis in 2002 because of chronic graft nephropathy. In 2005, a second dead donor kidney was grafted, with
the introduction of quadruple immunosuppression in the form of basiliximab, corticosteroids, mycophenolate mofetil
and tacrolimus. The subsequent course proved favorable, with creatinine clearance 75 ml/min (Cockroft-Gault). Four months after transplantation, the patient developed bilateral deep venous thrombosis and pulmonary thromboembolism. At that time kidney function remained stable, with normal lipid metabolism (cholesterol 213 mg/dl, triglycerides 163 mg/dl) and thyroid hormones, and normal thrombophilia findings. Treatment was provided in the form of tacrolimus, mycophenolate mofetil, prednisone, bisoprolol, furosemide and omeprazole. Anticoagulation was started with dalteparin 18,000 U/24 hours. The posterior controls showed a gradual increase in triglyceride levels (fig. 1); gemfibrozil was therefore started at increasing doses, associated to atorvastatin ¿ though with scant response. Due to the suspicion of hypertriglyceridemia secondary to dalteparin treatment, the latter was replaced with acenocoumarol. This was followed by a decrease in triglyceride levels, as a result of which the lipidlowering medication was gradually withdrawn (fig. 1).
Hypertriglyceridemia is a side effect of heparin administration. Our patient was obese, with grade II renal failure,
and was subjected to antihypertensive treatment (bisoprolol) and immunosuppression (corticosteroids and tacrolimus). All these hypertriglyceridemiacontributing factors were present before the start of treatment with dalteparin. From introduction of the latter drug, the triglyceride levels were found to be uncontrollable despite intensive medical care. Only dalteparin withdrawal proved effective.
We therefore conclude that dalteparin, one of the LMWHs with the most beneficial effects upon patient lipid profile,6 was the cause of severe hypertriglyceridemia in our case. This is an unusual side effect of LMWHs that nevertheless
must be taken into consideration by physicians, in view of the widespread use of both LMWHs and unfractionated
heparins. In addition, their use in patients at high cardiovascular risk must be carefully evaluated.
therefore important to address associated risk factors such as hyperlipidemia. The etiology of hypertriglyceridemia is influenced by obesity, diabetes mellitus, drugs (tacrolimus, β-blockers, corticosteroids, etc., alcohol consumption,
hypothyroidism, renal failure, nephrotic syndrome and HIV infection.1 Hypertriglyceridemia in the order of 2000
mg/dl is almost always of a secondary or familial origin.
Heparin is widely used as effective prophylaxis and treatment in patients with thrombosis. Independently of its
anticoagulant action, the administration of heparin gives rise to two opposite phenomena regarding the effect of the
drug on the patient lipid profile, derived from its action upon lipoprotein lipase: in the first hour, heparin stimulates the enzyme2 and reduces the triglyceride levels, while posteriorly the enzyme is inhibited and the triglyceride levels consequently increase.3 Although controversial, a number of studies have reported the favorable effects of low molecular weight heparins (LMWHs) upon lipid profile.4,5
We report the case of a 37-year-old male with a history of arterial hypertension, hypercholesterolemia, terminal
chronic renal failure secondary to reflow nephropathy and a first kidney transplant in 1984, with a return to hemodialysis in 2002 because of chronic graft nephropathy. In 2005, a second dead donor kidney was grafted, with
the introduction of quadruple immunosuppression in the form of basiliximab, corticosteroids, mycophenolate mofetil
and tacrolimus. The subsequent course proved favorable, with creatinine clearance 75 ml/min (Cockroft-Gault). Four months after transplantation, the patient developed bilateral deep venous thrombosis and pulmonary thromboembolism. At that time kidney function remained stable, with normal lipid metabolism (cholesterol 213 mg/dl, triglycerides 163 mg/dl) and thyroid hormones, and normal thrombophilia findings. Treatment was provided in the form of tacrolimus, mycophenolate mofetil, prednisone, bisoprolol, furosemide and omeprazole. Anticoagulation was started with dalteparin 18,000 U/24 hours. The posterior controls showed a gradual increase in triglyceride levels (fig. 1); gemfibrozil was therefore started at increasing doses, associated to atorvastatin ¿ though with scant response. Due to the suspicion of hypertriglyceridemia secondary to dalteparin treatment, the latter was replaced with acenocoumarol. This was followed by a decrease in triglyceride levels, as a result of which the lipidlowering medication was gradually withdrawn (fig. 1).
Hypertriglyceridemia is a side effect of heparin administration. Our patient was obese, with grade II renal failure,
and was subjected to antihypertensive treatment (bisoprolol) and immunosuppression (corticosteroids and tacrolimus). All these hypertriglyceridemiacontributing factors were present before the start of treatment with dalteparin. From introduction of the latter drug, the triglyceride levels were found to be uncontrollable despite intensive medical care. Only dalteparin withdrawal proved effective.
We therefore conclude that dalteparin, one of the LMWHs with the most beneficial effects upon patient lipid profile,6 was the cause of severe hypertriglyceridemia in our case. This is an unusual side effect of LMWHs that nevertheless
must be taken into consideration by physicians, in view of the widespread use of both LMWHs and unfractionated
heparins. In addition, their use in patients at high cardiovascular risk must be carefully evaluated.
